6 Viral Infections Flashcards
- a family of DNA viruses that affect humans exclusively
- endemic worldwide
- potential lifeline infection
- 8 different types
human herpesviruses
How do herpesviruses have the potential to be lifelong?
primary infection –> latency of the virus within specific cells –> ability to undergo reactivation
Compare/contrast HSV-1 and HSV-2
HSV-1
- tends to affect the oral, facial, and ocular regions
- spread through infected saliva or active lesions
HSV-2
- tends to affect the genital mucosa
- spread through sexual contact
Both
- structurally similar (50% DNA sequence homology)
- different epidemiology
- both types infect epithelial cells then establish latency in nerve ganglia
- clinical lesions appear the same, but different anatomic pattern distribution
- rarely, HSV-1 can cause a HSV-2-like anatomic pattern of infection (and vice versa)
How can being infected with HSV-1 help reduce the change of being infected by HSV-2?
antibodies directed against one type can cross-react with the other type
HSV-1: primary infection –> latency –> recurrent infection
Primary infection- often (but not always) asymptomatic
Latency- the trigeminal ganglion is the most common site of latency
Recurrent infection- asymptomatic viral shedding in the saliva (common), symptomatic recurrent infections (herpes labialis, recurrent intraoral herpes)
How is the HSV-1 primary infection contracted?
occurs by contact with an infected person who is actively releasing the virus (majority of primary infections are asymptomatic)
socioeconomic status and age of infection of HSV-1
Developing countries: 50% by age 5, 100% by age 30
Developed countries: 20% by age 5, 50-60% by adulthood
2 systemic primary infections of HSV-1
- acute herpetic gingivostomatitis
- pharyngotonsillitis (less common, adults, tonsils and pharynx only)
- most common type of symptomatic primary HSV-1 infection
- most cases develop between 6 months-5 years of age
- newborns are protected by maternal antibodies
- can be seen in teenagers and adults too
acute herpetic gingivostomatitis
peak prevalence of acute herpetic gingivostomatitis
2-3 years of age
clinical features: cervical lymphadenopathy, fever, chills, nausea, anorexia, painful oral lesions, abrupt onset
acute herpetic gingivostomatitis
Name the disease that these oral lesions describe:
- both moveable and attached mucosa affected
- numerous, tiny vesicles that rapidly rupture and coalesce to form larger areas of ulceration
- gingiva becomes enlarged, painful, and intensely erythematous
- erosion/ulceration is especially common at the free gingival margin
acute herpetic gingivotomatitis
occurs at areas supplied by the involved nerve ganglion (usually trigeminal)
recurrent HSV-1 infection
Most common site of recurrence of HSV-1?
Recurrences can also affect?
- vermillion border and perioral skin is the most common site of recurrence (herpes labialis)
- recurrences can also affect the oral mucosa (recurrent intraoral herpes)
aka “cold sores” or “fever blisters”, 15-45% of the US population has a history of this
herpes labialis
Potential triggers for herpes labialis:
- exposure to UV light (only one experimentally proven)
- physical or emotional stress
- trauma (including manipulation of tissues during dental procedures)
- characteristic prodrome 6-24 hours before clinical lesions develop (pain, burning, tingling, itching, erythema)
- clusters of fluid-filled vesicles form, rupture, and crust within 2 days
- mechanical rupture of intact vesicles can result in spreading of the virus
herpes labialis
recurrent intraoral herpes: involvement is limited to what parts of the mouth
keratinized, attached mucosa (attached gingiva, hard palate)
a cluster of tiny vesicles that quickly rupture to form shallow erosions and ulcers
recurrent intraoral herpes
HSV-1 infection of the thumbs and fingers, can occur through self-inoculation by a young patient who has primary herpes
herpetic whitlow
- before routine use of gloves, medical and dental professionals were commonly affected due to contact with infected patients
- recurrences on the fingers are common and can cause paresthesia and scarring
herpetic whitlow
Diagnosis of?
- clinical presentation is often characteristic
- exfoliative cytology or biopsy
HSV-1
In HSV-1, infected epithelial cells become ______ (detached from each other –> _____ cells)
acantholytic / Tzank cells
histo: enlarged and multinucleated epithelial cells
HSV-1
tx for HSV-1
antiviral meds, restrict contact with others, postpone dental treatment until resolved, pall
palliative care for HSV-1
- adequate hydration and nutrition
- tylenol or ibuprofen
- viscous lidocaine (adults only)
- dyclonine HCl 0.5-1% (kids)
treating acute herpetic gingivostomatitis (children)
acyclovir suspension (within first 3 days)
treating primary OR recurrent HSV-1 (adults and kids over 12)
valacyclovir (valtrex) 1 g caplets, initiate treatment during the prodrome or as early as possible in the course of the infection
topical cream (penciclovir 1% cream), start during prodrome
treating herpes labialis
HHV-3
varicella zoster virus (VZV)
How is VZV spread?
air droplets or direct contact with active lesions
primary vs recurrent VZV infection
Primary = varicella (chickenpox)
Recurrent = herpes zoster (shingles)
- primary VZV infection
- non-immunized patients
- clinical features: sore throat, runny nose, fever, characteristic itchy rash
chickenpox
distribution of lesions during chickenpox
skin lesions begin first on the face and trunk, then spread to the extremities
progression of each lesion with chickenpox
erythema –> vesicle –> pustule –> crust/scab
vesicle stage of chickenpox looks like this
“a dewdrop on a rose petal”
Potential complications of varicella (chickenpox) in children vs adults
Children
- skin infections
- encephalitis
- pneumonia
Adults
- occur more often than in kids
- most common and most serious = pneumonia
Those infected with varicella (chickenpox) are contagious from when to when?
from 2 days before the rash until all lesions have crusted
vaccination against varicella (chickenpox)
MMRV (2 doses: first at 12-15 months, second at age 4-6 years)
After the primary infection, VZV establishes latency where? What happens when VZV is reactivated?
nerves / herpes zoster (shingles)
involves the skin distribution of the affected sensory nerve (dermatome), affects 1 in 3 individuals during their lifetime, can occur more than once, incidence increases dramatically after age 50
herpes zoster (shingles)
3 phases of herpes zoster (shingles)
prodrome, acute, chronic
Name the phase of herpes zoster (shingles):
- Precedes the skin rash by 1-4 days
- Present in over 90% of cases
- PAIN in the area of skin innervated by the affected dermatome
- Thoracic dermatomes are affected in about 2/3s of cases
prodrome phase
Name the phase of herpes zoster (shingles):
- Affected skin develops clusters of vesicles with surrounding erythema
- Vesicles collapse and form crusts
- Lesions terminate at the midline!
- If the trigeminal nerve is affected, oral lesions can occur (usually the overlying skin is also involved)
- Resolves in 2-3 weeks
acute phase
Name the phase of herpes zoster (shingles):
- Characterized by postherpetic neuralgia
- Pain that persists more than 90 days after rash onset
- Rare in patients under age 40
- Affects at least 10-15% of patients over age 60
- Older adults are more likely to have severe and longer-lasting pain
chronic phase
vaccine against herpes zoster (singles) recommended for all people > 50 yo
shingrix vaccine
ocular involvement can cause blindness (what is the hint that an ocular infection exists?)
herpes zoster (shingles)
*Hint: if the tip of the nose is has lesions, V1 (ophthalmic division) is affected and the potential for ocular infection exists, referral to an opthalmologist is mandatory!
usually the worst aspect of a herpes zoster (shingles) infection and also the most difficult to successfully treat
postherpetic neuralgia
HHV-4
Epstein-Barr virus (EBV)
- Exposure during childhood is usually asymptomatic
- Most symptomatic primary infections occur in young adults (infectious mononucleosis)
- Symptomatic primary infection = Spread through contaminated saliva, intimate contact (“kissing disease”)
EBV
Where does EBV remain latent?
B lymphocytes
exposure of EBV in developing nations vs US
Developing: exposure usually occurs by age 3 (universal by adolescence)
US: exposure is delayed, 50% of entering college students are unexposed
EBV is also implicated in other diseases besides mononucleosis:
- oral hairy leukoplakia
- some lymphomas (especially Burkitt lymphoma)
- nasopharyngeal carcinoma
Clinical features:
- Prodrome of fatigue, malaise, anorexia (may precede other symptoms below by 2 weeks)
- Fever
- Pharyngitis
- Cervical lymphadenopathy (bilateral) –> occurs in over 90% of cases
- Hepatosplenomegaly
- Tonsillitis (diffuse surface exudate)
- Enlargement of both pharyngeal and lingual tonsils
- Palatal petechiae (present in 25% of cases)
- Necrotizing ulcerative gingivitis
mononucleosis
HHV-5
cytomegalovirus (CMV)
90% of primary infections (at any age) are asymptomatic
CMV
Where does CMV become latent?
After the primary infection, CMV can become latent in salivary gland cells, endothelium, macrophages, and lymphocytes.
Seroprevalence in U.S. population = 50% for individuals 6-49 years old
CMV
- Infants can become infected through the placenta, during delivery, or during nursing
- Another transmission peak occurs during adolescence (exchange of body fluids)
CMV
symptomatic infections are usually limited to newborns and immunosuppressed patients
CMV
Immunosuppressed patients affected by CMV:
- transplant patients
- AIDS patients (CMV chorioretinitis, CMV colitis)
histo: “owl eye” appearance
CMV
- RNA viruses associated with several diseases (coxsackieviruses A & B, echoviruses, poliovirus)
- Routes of transmission: fecal-oral (ingestion), saliva, respiratory droplets
- Very common (10-15 million infections/year in U.S.)
- Epidemics that affect children ages 1-4
enteroviruses
- Usually caused by one of the coxsackieviruses
- Most cases are mild and resolve within 1 week
herpangina
Clinical features:
- fever
- sore throat
- dysphagia
- a small amount (< 10) vesicles develop on the soft palate and tonsillar pillars, then rapidly ulcerate
herpangina
usually coxsackievirus A16
Hand-Foot-and-Mouth Disease
Clinical features:
- Fever, flu-like symptoms
- Oral lesions precede the development of skin lesions (may develop anywhere intraorally, variable in #)
- Individual vesicles that rupture to form ulcers
- Skin lesions: hands, feet, fingers and toes (red macules that develop central vesicles, may heal without crusting)
hand-foot-and-mouth disease
- Spread through respiratory droplets
- Highly contagious
- Pre-vaccine era (1963): >90% infected in U.S. by age 15
- Was declared “eliminated” from U.S. in 2000
- Still common in other countries
- Has made a comeback in the U.S. among unvaccinated individuals
- The MMRV vaccine is 99% effective
measles (rubeola)
Name the stage of measles infection: fever, cough, runny nose, conjunctivitis, Koplik’s spots (oral cavity)
first stage
- Areas of erythema with numerous small, blue/white macules (“grains of salt”)
- Buccal and labial mucosa, soft palate
Koplik’s spots (measles)
Name the stage of measles infection: fever continues, diffuse erythematous maculopapular skin rash “morbilliform”
measles
Name the stage of measles infection: fever ends, rash fades then desquamates
third stage
complications from measles
common in up to 40% of cases –> pneumonia, encephalitis (1 in 5 require hospitalization)
- Swelling and inflammation of exocrine glands
- Salivary glands are the best known site of involvement
- Spreads through urine, saliva, and respiratory droplets
- Epidemiology significantly affected by vaccination (88% effective)
- Epidemics that usually occur among adolescents and young adults
- 30% of cases are asymptomatic
mumps
- Rapid testicular swelling, pain, and tenderness
- Usually unilateral
- Affects 25% of post-pubertal males
orchitis (associated with mumps)
